ミダゾラムによる鎮静時のBispectral Index変化とfMRIによる脳機能画像の検討

抄録

Psychosedation, as used in the field of dentistry, is intended to provide trouble-free dental care while maintaining a proper level of sedation. One drug used in psychosedation is midazolam, which is known to have a strong amnestic effect. In the current research, I sought to clarify whether the bispectral index (BIS) using EEC analysis can be used for assessment of optimal sedation in psychosedation, and what effects midazolam has on the cerebrum's mechanism of memory. The subjects were 17 healthy adult volunteers. Intravenous sedation involved a single administration of 0.06mg/kg midazolam, or 6mg/kg/h propofol, administered for 5 minutes and then continuously administered for 25 minutes at 3mg/kg/h. For nitrous oxide inhalation sedation, 10-30% nitrous oxide was used. Clinical sedation and the BIS were measured in a variety of circumstances. To examine the effects of midazolam on the central nervous system, changes in brain oxygen consumption in visual memory tasks were assessed through observing changes in areas of brain activation using 3 T fMRI. With intravenous sedation using midazolam or propofol, the BIS decreased immediately after drug administration, and the BIS at which optimal sedation was clinically determined was about 65. In contrast, no decrease in the BIS was noted with nitrous oxide inhalation sedation. In observing areas of brain activation by fMRI, the oxygen consumption mainly of visual cortices in the occipital lobe increased as a result of stimulation by visual memory tasks. Regardless of the amnestic effect midazolam produced in subjects, it did not suppress activation of the visual cortices in the occipital lobe. In intravenous sedation using midazolam or propofol, the BIS is effective in determining optimal sedation, and appropriate perioperative management can be performed using the BIS. However, in nitrous oxide inhalation sedation it appears that the BIS cannot be used to monitor levels of sedation. Amnestic action by midazolam is assumed to occur not through inhibition of pathways from visual cells to visual cortices, but through inhibition of the higher central nervous system.